1964Journal of Cellular and Comparative PhysiologyRequires access

Virus defectiveness and cell transformation in the Rous sarcoma

H. Rubin

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Abstract

The Rous sarcoma virus (RSV) is unique among tumor viruses in the great speed and high frequency with which it induces the malignant transformation in the infected cell. It is also unique in its defectiveness — it cannot reproduce new, infectious virus particles unless a helper virus is present. Such a helper virus, known as RAV, occurs in stocks of the Bryan high titer strain of RSV. It is a member of the avian leukosis group of viruses. All the other avian leukosis viruses tested to date can substitute for RAV as helper viruses. An analysis has been carried out of the independent and helper-dependent functions of RSV. RSV carries out the malignant transformation of cells without the aid of helper virus and controls the morphology of the transformation. It also reproduces its own genetic material in solitary infection. However, it is completely dependent on helper virus for synthesis of its protein coat. As a result, RSV bears the antigenic identity of its helper virus. By using different helper viruses, it has been found that the ability of RSV to infect chicken cells of a given genetic constitution depends on the coat of the virus. In addition, the susceptibility of RSV to interference by leukosis viruses depends on similarity between the coat of the leukosis virus and that of the super-infecting RSV. The results to date indicate both these forms of cellular resistance to RSV are associated with the failure of RSV to penetrate the cell.

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What this paper is about

The Rous sarcoma virus (RSV) is unique among tumor viruses in the great speed and high frequency with which it induces the malignant transformation in the infected cell. It is also unique in its defectiveness — it cannot reproduce new, infectious virus particles unless a helper virus is present. Such a helper virus, known as RAV, occurs in stocks of the Bryan high titer strain of RSV. It is a member of the avian leukosis group of viruses. All the other avian leukosis viruses tested to date can substitute for RAV as helper viruses. An analysis has been carried out of the independent and helper-dependent functions of RSV. RSV carries out the malignant transformation of cells without the aid of helper virus and controls the morphology of the transformation. It also reproduces its own genetic material in solitary infection. However, it is completely dependent on helper virus for synthesis of its protein coat. As a result, RSV bears the antigenic identity of its helper virus. By using different helper viruses, it has been found that the ability of RSV to infect chicken cells of a given genetic constitution depends on the coat of the virus. In addition, the susceptibility of RSV to interference by leukosis viruses depends on similarity between the coat of the leukosis virus and that of the super-infecting RSV. The results to date indicate both these forms of cellular resistance to RSV are associated with the failure of RSV to penetrate the cell.

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Available abstract

The Rous sarcoma virus (RSV) is unique among tumor viruses in the great speed and high frequency with which it induces the malignant transformation in the infected cell. It is also unique in its defectiveness — it cannot reproduce new, infectious virus particles unless a helper virus is present. Such a helper virus, known as RAV, occurs in stocks of the Bryan high titer strain of RSV. It is a member of the avian leukosis group of viruses. All the other avian leukosis viruses tested to date can substitute for RAV as helper viruses. An analysis has been carried out of the independent and helper-dependent functions of RSV. RSV carries out the malignant transformation of cells without the aid of helper virus and controls the morphology of the transformation. It also reproduces its own genetic material in solitary infection. However, it is completely dependent on helper virus for synthesis of its protein coat. As a result, RSV bears the antigenic identity of its helper virus. By using different helper viruses, it has been found that the ability of RSV to infect chicken cells of a given genetic constitution depends on the coat of the virus. In addition, the susceptibility of RSV to interference by leukosis viruses depends on similarity between the coat of the leukosis virus and that of the super-infecting RSV. The results to date indicate both these forms of cellular resistance to RSV are associated with the failure of RSV to penetrate the cell.

Key concepts: Rous sarcoma virus, Virology, Virus, Helper virus, Biology, Viral transformation, Titer, Viral Interference

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